You Searched For: JNK-IN-8

Supplier: Biotium

Description: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

Supplier: Biotium

Description: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

Catalog Number: (BOSSBS-3353R-CY5.5)

Supplier: Bioss

Description: Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Phosphorylation of MAP3K5, an other proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promote cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post-translational levels. Phosphorylation of CDKN1B,induces 14-3-3-proteins binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis.

UOM: 1 * 100 µl

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Supplier: Biotium

Description: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

Supplier: Biotium

Description: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

Catalog Number: (BOSSBS-3353R-A647)

Supplier: Bioss

Description: Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Phosphorylation of MAP3K5, an other proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promote cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post-translational levels. Phosphorylation of CDKN1B,induces 14-3-3-proteins binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis.

UOM: 1 * 100 µl

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Catalog Number: (PRSI33-493)

Supplier: ProSci Inc.

Description: Recognises a protein of a disulfide-linked 120 kDa dimer, identified as CD27 (Workshop VI; Code 6T-028). CD27 is expressed on the majority of peripheral T cells, medullary thymocytes, memory-type B cells, and natural killer cells. It is a transmembrane phosphoglycoprotein that belongs to the tumor necrosis factor receptor (TNFR) superfamily. CD27 binds to its ligand CD70, a member of the TNF family, and induces T-cell co-stimulation and B-cell activation. It also interacts with TRAFs and is involved in activation of NFB and SAPK/JNK and induces apoptosis.

UOM: 1 * 100 µG

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Catalog Number: (BOSSBS-4162R-A680)

Supplier: Bioss

Description: The protein encoded by this gene is a member of the PP2C family of Ser/Thr protein phosphatases. PP2C family members are known to be negative regulators of cell stress response pathways. This phosphatase dephosphorylates, and negatively regulates the activities of, MAP kinases and MAP kinase kinases. It has been shown to inhibit the activation of p38 and JNK kinase cascades induced by environmental stresses. This phosphatase can also dephosphorylate cyclin-dependent kinases, and thus may be involved in cell cycle control. Overexpression of this phosphatase is reported to activate the expression of the tumor suppressor gene TP53/p53, which leads to G2/M cell cycle arrest and apoptosis. Three alternatively spliced transcript variants encoding distinct isoforms have been described.

UOM: 1 * 100 µl

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Supplier: Biotium

Description: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

Supplier: Biotium

Description: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

Supplier: Biotium

Description: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

Catalog Number: (BOSSBS-3353R-A488)

Supplier: Bioss

Description: Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Phosphorylation of MAP3K5, an other proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promote cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post-translational levels. Phosphorylation of CDKN1B,induces 14-3-3-proteins binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis.

UOM: 1 * 100 µl

Sale

Catalog Number: (BOSSBS-3353R-CY5)

Supplier: Bioss

Description: Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Phosphorylation of MAP3K5, an other proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promote cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post-translational levels. Phosphorylation of CDKN1B,induces 14-3-3-proteins binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis.

UOM: 1 * 100 µl

Sale

Catalog Number: (BOSSBS-3353R-A680)

Supplier: Bioss

Description: Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilisation of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Phosphorylation of MAP3K5, an other proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promote cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post-translational levels. Phosphorylation of CDKN1B,induces 14-3-3-proteins binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis.

UOM: 1 * 100 µl

Sale

Catalog Number: (BOSSBS-3353R-CY3)

Supplier: Bioss

Description: Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Phosphorylation of MAP3K5, an other proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promote cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post-translational levels. Phosphorylation of CDKN1B,induces 14-3-3-proteins binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis.

UOM: 1 * 100 µl

Sale

Supplier: Biotium

Description: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.